Vitamin B6 (B6) is an essential cofactor of glutamate decarboxylase and catalyzes the decarboxylation of the excitatory neurotransmitter glutamate to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Although immediate administration of B6 to patients with acute encephalopathy with febrile convulsive status epilepticus (AEFCSE) is effective, it is not known whether prolonged seizures in status epilepticus (SE) children prevent the transport of B6 to the central nervous system (CNS) and/or induce the consumption of B6 inside the CNS. We evaluated the B6 concentration in cerebrospinal fluid (CSF) and serum in SE children. Further, we performed a sequential serum B6 analysis on days 1 and 2 after admission and on the day before discharge. Among the several vitamers of B6, we used pyridoxal (PL) as a representative of B6 in this study. We enrolled 15 SE children (8 boys and 7 girls; age range,1-11years; average age, 3.3years) and 21 control children (3 boys and 18 girls; age range, 7months-14years; average age, 3.0years) and each group was divided into 2 subgroups according to age (4months-1year and 2-14years). We found no significant differences in the CSF PL levels, CSF/serum PL ratios, and serum PL levels in the SE and control subgroups. Our results suggest that prolonged seizures do not result in B6 deficiency in CSF and serum in SE children. Whenever necessary, B6 should be administered to SE children with caution to prevent possible adverse effects.
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